Additional file 1 of A hypoxia–glycolysis–lactate-related gene signature for prognosis prediction in hepatocellular carcinoma

Supplementary Material

Bimodal Phosphorescence–Magnetic Resonance Imaging Nanoprobes for Glutathione Based on MnO₂ Nanosheet–Ru(II) Complex Nanoarchitecture

Bimodal fluorescence–magnetic resonance imaging (MRI) technique has shown great utilities in bioassays because it combines the advantages of both optical imaging and MRI to provide more sufficient information over any modality alone. In this work, on the basis of a MnO2 nanosheet–Ru­(II) complex nanoarchitecture, a bimodal phosphorescence–MRI nanoprobe for glutathione (GSH) has been constructed. The nanoprobe, Ru­(BPY)3@MnO2, was constructed by integrating MnO2 nanosheets with a phosphorescent Ru­(II) complex [Ru­(BPY)3]­(PF6)2 (BPY = 2,2′-bipyridine), which resulted in complete phosphorescence quenching of the Ru­(II) complex, accompanied by very low longitudinal and transverse relaxivity. Upon exposure to GSH, the reduction of MnO2 nanosheets by GSH triggers a recovery of phosphorescence and simultaneously produces a number of Mn2+ ions, a perfect MRI contrast agent. The as-prepared nanoprobe showed good water dispersion and biocompatibility and a rapid, selective, and sensitive response toward GSH in the phosphorescence and MR detection modes. The practicability of the nanoprobe was proved by time-gated luminescence assay of GSH in human serum, phosphorescent imaging of endogenous GSH in living cells, zebrafish, and tumor-bearing mice, as well as the MRI of GSH in tumor-bearing mice. The research outcomes suggested the potential of Ru­(BPY)3@MnO2 for the bimodal phosphorescence–MRI sensing of GSH in vitro and in vivo

Table_1_Percutaneous angioplasty and/or stenting versus aggressive medical therapy in patients with symptomatic intracranial atherosclerotic stenosis: a 1-year follow-up study.docx

BackgroundSymptomatic intracranial atherosclerotic stenosis (sICAS) is one of the common causes of ischemic stroke. However, the treatment of sICAS remains a challenge in the past with unfavorable findings. The purpose of this study was to explore the effect of stenting versus aggressive medical management on preventing recurrent stroke in patients with sICAS.MethodsWe prospectively collected the clinical information of patients with sICAS who underwent percutaneous angioplasty and/or stenting (PTAS) or aggressive medical therapy from March 2020 to February 2022. Propensity score matching (PSM) was employed to ensure well-balanced characteristics of two groups. The primary outcome endpoint was defined as recurrent stroke or transient ischemic attack (TIA) within 1 year.ResultsWe enrolled 207 patients (51 in the PTAS and 156 in the aggressive medical groups) with sICAS. No significant difference was found between PTAS group and aggressive medical group for the risk of stroke or TIA in the same territory beyond 30 days through 6 months (P = 0.570) and beyond 30 days through 1 year (P = 0.739) except for within 30 days (P = 0.003). Furthermore, none showed a significant difference for disabling stroke, death and intracranial hemorrhage within 1 year. These results remain stable after adjustment. After PSM, all the outcomes have no significant difference between these two groups.ConclusionThe PTAS has similar treatment outcomes compared with aggressive medical therapy in patients with sICAS across 1-year follow-up.</p

Figure S2 from Metabolic Enzyme DLST Promotes Tumor Aggression and Reveals a Vulnerability to OXPHOS Inhibition in High-Risk Neuroblastoma

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Figure S3 from Metabolic Enzyme DLST Promotes Tumor Aggression and Reveals a Vulnerability to OXPHOS Inhibition in High-Risk Neuroblastoma

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Figure S4 from Metabolic Enzyme DLST Promotes Tumor Aggression and Reveals a Vulnerability to OXPHOS Inhibition in High-Risk Neuroblastoma

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Supplementary Data_v1 from Metabolic Enzyme DLST Promotes Tumor Aggression and Reveals a Vulnerability to OXPHOS Inhibition in High-Risk Neuroblastoma

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Figure S1 from Metabolic Enzyme DLST Promotes Tumor Aggression and Reveals a Vulnerability to OXPHOS Inhibition in High-Risk Neuroblastoma

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Figure S6 from Metabolic Enzyme DLST Promotes Tumor Aggression and Reveals a Vulnerability to OXPHOS Inhibition in High-Risk Neuroblastoma

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Figure S5 from Metabolic Enzyme DLST Promotes Tumor Aggression and Reveals a Vulnerability to OXPHOS Inhibition in High-Risk Neuroblastoma

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